Studies have reported low seroconversion rates (58% after the second dose) in solid organ transplant recipients who received a messenger RNA (mRNA) SARS-CoV-2 vaccine. 1,2 Based on this evidence, the French National Authority for Health issued a recommendation in April 2021 to administer a third vaccine dose in immunosuppressed patients who did not respond after 2 doses. We examined the antibody responses of kidney transplant recipients who did not respond to 2 doses and received a third dose (100 μg) of the mRNA-1273 vaccine (Moderna).
Background
Neurological manifestations in coronavirus disease (COVID)‐2019 may adversely affect clinical outcomes. Severe COVID‐19 and uremia are risk factors for neurological complications. However, the lack of insight into their pathogenesis, particularly with respect to the role of the cytokine release syndrome (CRS), is currently hampering effective therapeutic interventions.
Methods
In this longitudinal study, we sought to describe the neurological manifestations of patients with COVID‐19 and gain pathophysiological insights especially with respect to the CRS. Extensive clinical, laboratory, and imaging phenotyping was performed in five patients admitted to our renal unit.
Results
Neurological presentation included confusion, tremor, cerebellar ataxia, behavioral alterations, aphasia, pyramidal syndrome, coma, cranial nerve palsy, dysautonomia, and central hypothyroidism. Neurological disturbances were remarkably accompanied by laboratory evidence of CRS. SARS‐CoV‐2 was undetectable in the cerebrospinal fluid (CSF). Hyperalbuminorrachia and increased levels of the astroglial protein S100B were suggestive of blood‐brain barrier (BBB) dysfunction. Brain MRI findings comprised evidence of acute leukoencephalitis (n = 3, of whom one with a hemorrhagic form), cytotoxic edema mimicking ischemic stroke (n = 1), or normal results (n = 2). Treatment with corticosteroids and/or intravenous immunoglobulins was attempted – resulting in rapid recovery from neurological disturbances in two cases. SARS‐CoV2 was undetectable in 88 of the 90 patients with COVID‐19 who underwent RT‐PCR testing of CSF.
Conclusions
Patients with COVID‐19 can develop neurological manifestations that share clinical, laboratory, and imaging similarities with those of chimeric antigen receptor‐T cell‐related encephalopathy. The pathophysiological underpinnings appear to involve CRS, endothelial activation, BBB dysfunction, and immune‐mediated mechanisms.
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